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A team of researchers at the Mayo Clinic has identified a previously unknown process inside aging cells that may help explain why chronic inflammation becomes more common as people grow older. The discovery could eventually lead to new therapies aimed at reducing the inflammation associated with heart disease, Alzheimer’s disease, arthritis, and other age-related illnesses. 

The research, published in the journal Nature, focuses on senescent cells, often called “zombie cells.” These are cells that have stopped dividing but do not die. Instead, they remain in the body and release inflammatory chemicals that can damage nearby healthy tissue. Scientists have long believed these cells contribute to many of the health problems associated with aging. 

The Mayo team discovered that malfunctioning mitochondria — the tiny structures inside cells that produce energy — play a much larger role in this process than previously understood.

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A new link between energy production and inflammation

Researchers found that damaged mitochondria increase the production of a molecule called acetyl-CoA. That molecule alters the way DNA is packaged inside the cell through a process known as epigenetic regulation, effectively switching on genes that produce inflammatory signals. 

In other words, aging mitochondria do more than generate less energy. They also appear to help “flip the switch” that tells senescent cells to produce chronic inflammation.

The researchers identified a mitochondrial transporter that plays a key role in this chain of events. In laboratory experiments, blocking that transporter reduced inflammatory activity without killing the senescent cells themselves.

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Why it matters for older adults

Low-grade, persistent inflammation — sometimes called “inflammaging” — is considered one of the major biological drivers of aging. Scientists believe it contributes to a wide range of diseases, including cardiovascular disease, type 2 diabetes, certain cancers, arthritis, and neurodegenerative disorders such as Alzheimer’s disease. 

Current experimental approaches often focus on eliminating senescent cells altogether using drugs known as senolytics. While promising, those treatments may not be appropriate for everyone because senescent cells can also play useful roles, such as helping wounds heal and preventing damaged cells from becoming cancerous. 

The newly discovered pathway raises the possibility of a different strategy: calming the harmful inflammatory signals while leaving the cells themselves intact.

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More research needed

The findings are encouraging, but they are still in the early stages. The work was conducted in laboratory models, and researchers caution that much more testing will be needed before any therapy based on the discovery could be evaluated in people.

Even so, the study provides scientists with a new target for developing drugs that could one day help reduce chronic inflammation and promote healthier aging.

For older adults, the research offers another piece of the puzzle in understanding why the risk of many chronic diseases increases with age — and how future treatments might help people stay healthier longer.